PT  - JOURNAL ARTICLE
AU  - Ghosh, Sangeeta
AU  - Patel, Nishant
AU  - Rahn, Douglas
AU  - McAllister, Jenna
AU  - Sadeghi, Sina
AU  - Horwitz, Geoffrey
AU  - Berry, Diana
AU  - Wang, Kai Xuan
AU  - Swerdlow, Russell H.
TI  - The Thiazolidinedione Pioglitazone Alters Mitochondrial Function in Human Neuron-Like Cells
AID  - 10.1124/mol.106.033845
DP  - 2007 Jun 01
TA  - Molecular Pharmacology
PG  - 1695--1702
VI  - 71
IP  - 6
4099  - http://molpharm.aspetjournals.org/content/71/6/1695.short
4100  - http://molpharm.aspetjournals.org/content/71/6/1695.full
SO  - Mol Pharmacol2007 Jun 01; 71
AB  - Thiazolidinediones alter cell energy metabolism. They are used to treat or are being considered for the treatment of disorders that feature mitochondrial impairment. Their mitochondrial effects, however, have not been comprehensively studied under long-term exposure conditions. We used the human neuron-like NT2 cell line to directly assess the long-term effects of a thiazolidinedione drug, pioglitazone, on mitochondria. At micromolar concentrations, pioglitazone increased mitochondrial DNA (mtDNA) content, levels of mtDNA and nuclear-encoded electron transport chain subunit proteins, increased oxygen consumption, and elevated complex I and complex IV Vmax activities. Pioglitazone treatment was also associated with increased cytoplasmic but reduced mitochondrial peroxide levels. Our data suggest that pioglitazone induces mitochondrial biogenesis and show that pioglitazone reduces mitochondrial oxidative stress in a neuron-like cell line. For these reasons pioglitazone may prove useful in the treatment of mitochondriopathies. The American Society for Pharmacology and Experimental Therapeutics